The PET1-CMS Mitochondrial Mutation in Sunflower Is Associated with Premature Programmed Cell Death and Cytochrome c Release

2001 ◽  
Vol 13 (8) ◽  
pp. 1803 ◽  
Author(s):  
Janneke Balk ◽  
Christopher J. Leaver
Keyword(s):  
Cell Death ◽  
Cytochrome C ◽  
Programmed Cell Death ◽  
Cytochrome C Release ◽  
Mitochondrial Mutation

Yeast acetic acid-induced programmed cell death can occur without cytochrome c release which requires metacaspase YCA1

FEBS Letters ◽  
2009 ◽  
Vol 584 (1) ◽  
pp. 224-228 ◽  
Author(s):  
Nicoletta Guaragnella ◽  
Antonella Bobba ◽  
Salvatore Passarella ◽  
Ersilia Marra ◽  
Sergio Giannattasio
Keyword(s):  
Cell Death ◽  
Acetic Acid ◽  
Cytochrome C ◽  
Programmed Cell Death ◽  
Cytochrome C Release

Cyclosporin A inhibits programmed cell death and cytochrome c release induced by fusicoccin in sycamore cells

PROTOPLASMA ◽  
2007 ◽  
Vol 231 (3-4) ◽  
pp. 193-199 ◽  
Author(s):  
N. Contran ◽  
R. Cerana ◽  
P. Crosti ◽  
M. Malerba
Keyword(s):  
Cell Death ◽  
Cytochrome C ◽  
Programmed Cell Death ◽  
Cyclosporin A ◽  
Cytochrome C Release

scholarly journals Apaf-1 and caspase-9 accelerate apoptosis, but do not determine whether factor-deprived or drug-treated cells die

2004 ◽  
Vol 165 (6) ◽  
pp. 835-842 ◽  
Author(s):  
Paul G. Ekert ◽  
Stuart H. Read ◽  
John Silke ◽  
Vanessa S. Marsden ◽  
Hitto Kaufmann ◽  
...  
Keyword(s):  
Cell Death ◽  
Growth Factor ◽  
Cytochrome C ◽  
Programmed Cell Death ◽  
Plasma Membranes ◽  
Mitochondrial Cytochrome ◽  
Caspase 9 ◽  
Cytochrome C Release ◽  
Caspase 2

Apoptosis after growth factor withdrawal or drug treatment is associated with mitochondrial cytochrome c release and activation of Apaf-1 and caspase-9. To determine whether loss of Apaf-1, caspase-2, and caspase-9 prevented death of factor-starved cells, allowing them to proliferate when growth factor was returned, we generated IL-3–dependent myeloid lines from gene-deleted mice. Long after growth factor removal, cells lacking Apaf-1, caspase-9 or both caspase-9 and caspase-2 appeared healthy, retained intact plasma membranes, and did not expose phosphatidylserine. However, release of cytochrome c still occurred, and they failed to form clones when IL-3 was restored. Cells lacking caspase-2 alone had no survival advantage. Therefore, Apaf-1, caspase-2, and caspase-9 are not required for programmed cell death of factor-dependent cells, but merely affect its rate. In contrast, transfection with Bcl-2 provided long-term, clonogenic protection, and could act independently of the apoptosome. Unlike expression of Bcl-2, loss of Apaf-1, caspase-2, or caspase-9 would therefore be unlikely to enhance the survival of cancer cells.

scholarly journals Cytochrome c Release and Mitochondria Involvement in Programmed Cell Death Induced by Acetic Acid in Saccharomyces cerevisiae

2002 ◽  
Vol 13 (8) ◽  
pp. 2598-2606 ◽  
Author(s):  
Paula Ludovico ◽  
Fernando Rodrigues ◽  
Agostinho Almeida ◽  
Manuel T. Silva ◽  
Antoni Barrientos ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Acetic Acid ◽  
Cytochrome C ◽  
Programmed Cell Death ◽  
Yeast Cells ◽  
Cytochrome C Release ◽  
Apoptotic Pathway ◽  
Enzymatic Assays ◽  
Species Production

Evidence is presented that mitochondria are implicated in the previously described programmed cell death (PCD) process induced by acetic acid in Saccharomyces cerevisiae. In yeast cells undergoing a PCD process induced by acetic acid, translocation of cytochrome c (CytC) to the cytosol and reactive oxygen species production, two events known to be proapoptotic in mammals, were observed. Associated with these events, reduction in oxygen consumption and in mitochondrial membrane potential was found. Enzymatic assays showed that the activity of complexbc 1 was normal, whereas that of cytochrome c oxidase (COX) was strongly decreased. This decrease is in accordance with the observed reduction in the amounts of COX II subunit and of cytochromesa+a 3 . The acetic acid-induced PCD process was found to be independent of oxidative phosphorylation because it was not inhibited by oligomycin treatment. The inability ofS. cerevisiae mutant strains (lacking mitochondrial DNA, heme lyase, or ATPase) to undergo acetic acid-induced PCD and in the ATPase mutant (knockout in ATP10) the absence of CytC release provides further evidence that the process is mediated by a mitochondria-dependent apoptotic pathway. The understanding of the involvement of a mitochondria-dependent apoptotic pathway inS. cerevisiae PCD process will be most useful in the further elucidation of an ancestral pathway common to PCD in metazoans.

Sign in / Sign up

Export Citation Format

Share Document